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Antisynthetase syndrome

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Anti-synthetase syndrome
Other namesAnti-Jo1 syndrome, AS syndrome, ASS
End-stage interstitial lung disease
SpecialtyImmunology
SymptomsFever, myositis, polyarthritis, interstitial lung disease, mechanic's hands, and Raynaud phenomenon.[1]
Differential diagnosisDermatomyositis, Immune-mediated necrotizing myopathy, and Polymyositis.[2]
TreatmentGlucocorticosteroids, immunosuppressive medications.[1]
Frequency1 in 25,000–33,000 worldwide[2]

Antisynthetase syndrome (ASS) is a multisystematic autoimmune disease associated with inflammatory myositis, interstitial lung disease, and antibodies directed against various synthetases of aminoacyl-transfer RNA.[3] Other common symptoms include mechanic's hands, Raynaud's phenomenon, arthritis, and fever.[4]

It is still unknown what causes interstitial lung disease associated with antisynthetase syndrome.[5] Many antisynthetase antibodies have been reported with anti-Jo1 being the most prevalent.[6] Pulmonary involvement is an important factor of morbidity and mortality with Antisynthetase syndrome, affecting 70–100% of patients.[7]

Antisynthetase syndrome is diagnosed by a combination of radiologic features, clinical criteria, and identification of aminoacyl tRNA synthetase antibodies.[8] Immunosuppressive medications such as mycophenolate mofetil, azathioprine, and tacrolimus are often used alongside corticosteroids to manage myositis and other pulmonary symptoms.[9]

It is believed that the mortality rate for antisynthetase syndrome is significantly higher than that of the general population.[10] The estimated cumulative ten-year survival rate for patients with different antisyntetase antibodies is 76.8%.[11]

Antisynthetase syndrome is estimated by Orphanet to affect 1–3 people per 100,000 worldwide; however, precise data on the disease's prevalence is not available.[12] Antisynthetase syndrome is more common in women.[13]

Signs and symptoms

[edit]

67–100% of those with antisynthetase syndrome have interstitial lung disease[13] with dyspnea and cough being the most common symptoms.[14] Pulmonary symptoms may present early on, alongside other symptoms or they may manifest later in the progression of antisynthetase syndrome.[15] A recent study showed that pleural involvement is often associated with antisynthetase syndrome, reporting that 42.2% patients with antisynthetase syndrome had pleural effusions.[16]

91% of patients with antisynthetase syndrome displayed myopathic muscular weakness.[13] Myositis is more commonly seen in those with anti-Jo1 than other antibodies.[17] Myopathy in antisynthetase syndrome can range from subclinical to substantial proximal weakness causing difficulties climbing stairs, reaching overhead cupboards, or getting up from a seated position.[18] 30.4–88.9% of those with antisynthetase syndrome report persistent muscular tenderness and myalgia.[19][20]

In antisynthetase syndrome, arthritis is commonly described as a symmetrical, non-erosive polyarthritis of the small hands and feet that can sometimes mimic CTD-associated, rheumatoid, and seronegative inflammatory arthritis.[21] Arthritis is non-specific and occurs in about 18–55% of Idiopathic inflammatory myopathies.[21] Arthritis is the presenting symptom in about 24–66% of patients which can often lead to diagnostic delays.[3] Hand X-ray lesions such as erosions, periarticular calcifications, and subluxations are seen in about 50% of patients.[22]

Raynaud's phenomenon is an episodic vasospasm of the toes and fingers usually precipitated by exposure to cold temperatures.[23] Raynaud's phenomenon can be primary or secondary to another disease.[24]

The term "mechanics hands" describes the roughening and cracking of the skin on the lateral sides of the fingers, usually the thumb's ulnar border and the index finger's radial border. Interface psoriasiform dermatitis is seen on biopsy.[25]

Dermatomyositis-like rashes are seen in 32–44% of those with antisynthetase syndrome. This includes heliotropic rash, Gottron papules, and lesions of the psoriasiform type that span the hand's dorsum and resemble the morphology of mechanics hands.[26]

Fever is reported in 21–66% of those with antisynthetase syndrome.[27][28]

Cardiac involvement such as pulmonary hypertension[29] and myocarditis[30] have also been reported. Other reported manifestations include sicca symptoms and dysphagia.[31]

Pathogenesis

[edit]

It is postulated that autoantibodies are formed against aminoacyl-tRNA synthetases. The synthetases may be involved in recruiting antigen-presenting and inflammatory cells to the site of muscle or lung injury. The specific molecular pathway of the process awaits elucidation.[18]

Antisynthetase antibodies

[edit]

The most common antibody is "Anti-Jo-1" named after John P, a patient with polymyositis and interstitial lung disease detected in 1980.[32] This anti-histidyl tRNA Synthetase antibody is commonly seen in patients with pulmonary manifestations of the syndrome. The following are other possible antibodies that may be seen in association with antisynthetase syndrome: Anti-PL-7, Anti-PL-12, Anti-EJ, Anti-OJ, Anti-KS, Anti-Zo, Anti-Ha (YRS, Tyr).[33]

Diagnosis

[edit]

The diagnostic criteria for antisynthetase syndrome include one or more anti-synthetase antibodies as well inflammatory polyarthritis that affects the small joints, inflammatory myopathy, or interstitial lung disease.[34]

A wide range of associated autoantibodies and myositis-specific antibodies have been found in those with idiopathic inflammatory myopathies and are often tested when evaluating idiopathic inflammatory myopathy.[35] Anti-synthetase antibodies specific to myositis are the defining feature of anti-synthetase syndrome. Anti-histidyl-tRNA synthetase and anti-Jo-1 are the most commonly found anti-synthetase antibodies. Less common antibodies include anti-EJ, anti-OJ, anti-PL12, and anti-PL7.[9]

The diagnosis of idiopathic interstitial lung disease can also involve testing for other myositis-specific autoantibodies such as anti-MDA5 autoantibodies,[36] anti-Mi-2 autoantibodies, and anti-signal recognition particle autoantibodies.[37] Autoantibodies often tested include anti-Ro/SSA,[38] anti-nuclear antibody, anti-U1-RNP, anti-Ku, and anti-PM-Scl.[37] Although anti-La/SSB and anti-Ro/SSA are often associated with Sjogren's syndrome they have been associated with antisynthetase syndrome and severe fibrotic idiopathic interstitial lung disease by high-resolution computed tomography.[39]

High-resolution computed tomography is common in the management and workup of interstitial lung disease. One study showed that reticulation, ground glass opacities, and traction bronchiectasis are the most common CT scan features of antisynthetase syndrome.[40] The presence of organizing pneumonia and non-specific interstitial pneumonia is somewhat common in antisynthetase syndrome.[41]

Lung biopsy is rarely performed when evaluating patients with antisynthetase syndrome since the diagnosis is usually made by a combination of symptoms, physical examination, high-resolution computed tomography findings, pulmonary function tests, and serologic data.[9] One study that analyzed the histopathologic findings using lung biopsies in patients with anti-PL7 antibodies and anti-Jo-1 antibodies found that 35% of patients had usual interstitial pneumonia and 50% had diffuse alveolar damage.[42]

Because interstitial lung disease is the main finding and myositis is often mild, muscle biopsy is rarely performed.[9] Although muscle biopsy is often helpful in other forms of idiopathic inflammatory myopathies, there is currently no evidence to support the use of muscle biopsy when diagnosing antisynthetase syndrome.[43]

Treatment

[edit]

The first line of treatment for idiopathic inflammatory myopathies is usually corticosteroids. However, when corticosteroids are tapered down there is often lung disease recurrence. Other immunosuppressive drugs can be added as corticosteroid-sparing agents or for refractory lung and muscle disease. Cyclophosphamide, rituximab, tacrolimus, mycophenolate mofetil, and azathioprine are often used alongside corticosteroids however there is no agreement as to which medication is preferred.[9]

No controlled trials have been performed to prove the superiority of corticosteroids compared to other immunosuppressive drugs in the treatment of antisynthetase syndrome. Those with antisynthetase syndrome often need multimodality treatment with frequent lung function monitoring.[44]

By inhibiting purine synthesis along with incorporating metabolites into DNA, azathioprine reduces immune function by preventing replication, especially of immune cells. Azathioprine is often used in the treatment of inflammatory myopathy and interstitial lung disease, especially when there is no response to corticosteroids. Azathioprine is typically used in combination with prednisone as a maintenance therapy.[45]

Mycophenolate mofetil changes purine synthesis to prevent lymphocytes from multiplying. It is often used after transplants to avoid rejection and is also used to treat connective tissue disorders. Studies have shown its efficacy and safety in patients with connective tissue disorders and interstitial lung disease.[46]

Tacrolimus and cyclosporine, two calcineurin inhibitors, work against the immune system by inhibiting T cells. One study showed that when patients with anti-Jo-1 antibodies received cyclosporine they displayed improved diffusing capacity for carbon monoxide and forced vital capacity.[47] A 1999 study reported that tacrolimus successfully treats polymyositis with interstitial lung disease.[48] Since then, many studies have suggested that tacrolimus is successful in treating patients with connective tissue disorders and inflammatory myopathy related interstitial lung disease.[49] It has also been used in combination with other immunosuppressive drugs and corticosteroids.[50] In patients with antisynthetase syndrome related interstitial lung disease tacrolimus has been demonstrated to improve muscle symptoms and lung function.[51]

Rituximab is a monoclonal antibody that specifically targets B-lymphocytes' CD20 surface antigen. One case series reported increased forced vital capacity in patients with antisynthetase syndrome-related interstitial lung disease who were treated with rituximab.[52] Another study showed improvements in lung function and/or respiratory symptoms in patients who has interstitial lung disease due to connective tissue disorders. Half of the patients had anti-Jo-1 antibodies.[53]

Cyclophosphamide is a cytotoxic agent that inhibits proliferation by alkylating DNA. It is usually only used to treat severe inflammatory myopathy and interstitial lung disease, especially acute respiratory distress syndrome, due to the severe nature of many of the possible side effects. Numerous case series have shown its effectiveness in treating inflammatory myopathy with and without interstitial lung disease.[54][55]

Although its precise mode of action is unknown, intravenous immunoglobulin (IVIG), a blood product made up of donated blood's pooled immunoglobulin G antibodies, is used to treat a variety of autoimmune and immune deficiency diseases. Patients with dermatomyositis who received IVIG showed a significant improvement in their symptoms and muscle strength in a randomized, placebo-controlled trial of the treatment.[56] Another case report suggests that IVIG can be effective in treating interstitial lung disease related to inflammatory myopathy.[57]

A case study has reported that the use of CD19-targeting CAR T cell therapy (originally used to treat lymphoma and leukemia) in a patient with refractory anti-synthetase syndrome had complete clinical remission during 200 days of follow-up post-infusion when the patient received with chimeric antigen receptor (CAR) T cells that recognize CD19+ B cells.[58] This shows that CD19-targeting CAR T cells could be a new therapy for patients who do not respond to the first-line immunosuppressive drugs.[59]

If there is esophageal involvement, gastric intubation or percutaneous endoscopic gastrostomy may be required.[60] Owing to severe interstitial lung disease, 14% of those with anti-Jo-1 or anti-PL-7 antibodies need oxygen therapy.[17] Rarely, medication is not successful and a lung transplant is necessary.[61] Patients with myositis should be advised to engage in individually tailored physical exercise because it lowers activity restrictions and has an anti-inflammatory effect.[62]

Outlook

[edit]

Antisynthetase syndrome mortality is thought to be substantially higher than that of the general population.[10] Patients who had various antisyntetase antibodies had an estimated cumulative ten-year survival rate of 76.8%.[11] Respiratory complications, infectious diseases like pneumonia, cancer,[60] cardiovascular disorders,[63] severe myositis, and interstitial lung disease are the main causes of death amongst anti Jo-1-positive patients.[10]

Risk factors for severe antisynthetase syndrome include calcinosis, esophageal involvement, cancer, interstitial lung disease without myositis, severe respiratory involvement, and older age at the time of diagnosis.[10] Muscle weakness and arthritis at the point of diagnosis have been noted as favorable outcome measures.[63]

One study reported that anti-PL-12 and anti-PL-7 antibodies were associated with a worse prognosis.[29] A large portion of deaths occurred during the first year of onset and mostly involved those with anti-PL-7.[10][63] Interstitial lung disease often led to deadly prognosis in comparison to anti-Jo1-positive patients with interstitial lung disease. Those with anti-Jo1 antibodies had less remission of myositis and more relapses than those with anti-PL-12 and anti-PL-7 antibodies.[64] Anti-Jo-1 and anti-Ro52 antibodies co-occurring were linked to an increased risk of neoplasm, a symptomatic severe variant of interstitial lung disease, myositis, and arthritis exacerbation.[20]

Although dermatomyositis has long been linked to an elevated risk of cancer, there is insufficient data to support this association when evaluating individuals who have antisynthetase syndrome for potential cancer.[9] The first documented case of antisynthetase syndrome linked to cancer occurred in 2008, involving a 59-year-old patient diagnosed with colon adenocarcinoma.[65] There have been numerous case reports along with case series since, with significantly different prevalence rates up to about 14%.[66][67] The frequency of cancer within three years of the anti-synthetase syndrome diagnosis was only 1.7% in a more comprehensive retrospective analysis involving 233 patients with the condition, which the authors claim was not significantly different from the population as a whole.[17] Age-appropriate cancer screening should be followed by healthcare providers for these patients, according to these studies, but there is no evidence to support further or non-guideline-based assessments. Case reports have shown that treating the underlying cancer can improve myositis as well as interstitial lung disease, which supports the theory that idiopathic inflammatory myopathy may be a paraneoplastic syndrome.[68]

Epidemiology

[edit]

Orphanet estimates that the global rate of antisynthetase syndrome is 1–9/100 000; however, exact information regarding the disease's prevalence is not available.[12] 11.1%[69] to 39.19% of those with idiopathic inflammatory myopathy have antisynthetase antibodies.[70] The EuroMyositis registry indicates that antisynthetase syndrome is more common than immune-mediated necrotizing myopathy and sporadic inclusion body myositis, but less common than dermatomyositis and polymyositis. Similar to other subtypes of idiopathic inflammatory myopathy, except for sporadic inclusion body myositis, antisynthetase syndrome is more common in women, with an estimated female-to-male ratio of roughly 7:3. In patients with dermatomyositis and polymyositis, the mean age at disease onset is 48 years, which is older than in patients with immune-mediated necrotizing myopathy and sporadic inclusion body myositis.[13]

References

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  1. ^ a b Sobarun P. "Antisynthetase syndrome". DermNet. Retrieved December 1, 2023.
  2. ^ a b Cai C (May 26, 2021). "Antisynthetase syndrome associated myositis". Pathology Outlines. Retrieved December 1, 2023.
  3. ^ a b Cavagna L, Nuño L, Scirè CA, Govoni M, Longo FJ, Franceschini F, et al. (February 2017). "Serum Jo-1 Autoantibody and Isolated Arthritis in the Antisynthetase Syndrome: Review of the Literature and Report of the Experience of AENEAS Collaborative Group". Clinical Reviews in Allergy & Immunology. 52 (1). Springer Science and Business Media LLC: 71–80. doi:10.1007/s12016-016-8528-9. PMID 26782036. S2CID 34446814. Retrieved December 4, 2023.
  4. ^ Sreevilasan SK, Devarasetti P, Narahari NK, Desai A, Rajasekhar L (November 2021). "Clinical profile and treatment outcomes in antisynthetase syndrome: a tertiary centre experience". Rheumatology Advances in Practice. 5 (Suppl 2). Oxford University Press (OUP): ii10–ii18. doi:10.1093/rap/rkab054. PMC 8570161. PMID 34755025.
  5. ^ Zhao, Na; Jiang, Wei; Wu, Hongliang; Wang, Ping; Wang, Xiaoni; Bai, Yu; Li, Yao; Tang, Yanchun; Liu, Ying (August 10, 2022). "Clinical features, prognostic factors, and survival of patients with antisynthetase syndrome and interstitial lung disease". Frontiers in Immunology. 13. Frontiers Media SA. doi:10.3389/fimmu.2022.872615. ISSN 1664-3224. PMC 9399497. PMID 36032132.
  6. ^ Marguerie C, Bunn CC, Beynon HL, Bernstein RM, Hughes JM, So AK, Walport MJ (October 1990). "Polymyositis, pulmonary fibrosis and autoantibodies to aminoacyl-tRNA synthetase enzymes". The Quarterly Journal of Medicine. 77 (282). Oxford University Press (OUP): 1019–1038. doi:10.1093/qjmed/77.1.1019. PMID 2267280. Retrieved December 4, 2023.
  7. ^ Stanciu R, Guiguet M, Musset L, Touitou D, Beigelman C, Rigolet A, et al. (September 2012). "Antisynthetase syndrome with anti-Jo1 antibodies in 48 patients: pulmonary involvement predicts disease-modifying antirheumatic drug use". The Journal of Rheumatology. 39 (9): 1835–1839. doi:10.3899/jrheum.111604. PMID 22859355.
  8. ^ Wells M, Alawi S, Thin KY, Gunawardena H, Brown AR, Edey A, et al. (September 14, 2022). "A multidisciplinary approach to the diagnosis of antisynthetase syndrome". Frontiers in Medicine. 9. Frontiers Media SA: 959653. doi:10.3389/fmed.2022.959653. PMC 9515890. PMID 36186825.
  9. ^ a b c d e f Witt LJ, Curran JJ, Strek ME (September 2016). "The Diagnosis and Treatment of Antisynthetase Syndrome". Clinical Pulmonary Medicine. 23 (5). Ovid Technologies (Wolters Kluwer Health): 218–226. doi:10.1097/cpm.0000000000000171. PMC 5006392. PMID 27594777.
  10. ^ a b c d e Trallero-Araguás, Ernesto; Grau-Junyent, Josep María; Labirua-Iturburu, Anne; García-Hernández, Francisco José; Monteagudo-Jiménez, Manuel; Fraile-Rodriguez, Guadalupe; Les-Bujanda, Iñigo; Rodriguez-Carballeira, Mónica; Sáez-Comet, Luis; Selva-O'Callaghan, Albert (2016). "Clinical manifestations and long-term outcome of anti-Jo1 antisynthetase patients in a large cohort of Spanish patients from the GEAS-IIM group". Seminars in Arthritis and Rheumatism. 46 (2). Elsevier BV: 225–231. doi:10.1016/j.semarthrit.2016.03.011. ISSN 0049-0172. PMID 27139168. Retrieved December 4, 2023.
  11. ^ a b Shi, Jingli; Li, Shanshan; Yang, Hanbo; Zhang, Yamei; Peng, Qinglin; Lu, Xin; Wang, Guochun (May 1, 2017). "Clinical Profiles and Prognosis of Patients with Distinct Antisynthetase Autoantibodies". The Journal of Rheumatology. 44 (7): 1051–1057. doi:10.3899/jrheum.161480. ISSN 0315-162X. PMID 28461650. S2CID 13757950. Retrieved December 4, 2023.
  12. ^ a b "Orphanet: Antisynthetase syndrome". Orphanet. December 4, 2023. Retrieved December 4, 2023.
  13. ^ a b c d Lilleker JB, Vencovsky J, Wang G, Wedderburn LR, Diederichsen LP, Schmidt J, et al. (January 2018). "The EuroMyositis registry: an international collaborative tool to facilitate myositis research". Annals of the Rheumatic Diseases. 77 (1): 30–39. doi:10.1136/annrheumdis-2017-211868. PMC 5754739. PMID 28855174.
  14. ^ Cojocaru M, Cojocaru IM, Chicos B (June 2016). "New Insights into Antisynthetase Syndrome". Maedica. 11 (2). Amaltea Medical, Editura Magister: 130–135. PMC 5394574. PMID 28461832.
  15. ^ Masiak A, Marzec M, Kulczycka J, Zdrojewski Z (February 28, 2020). "The clinical phenotype associated with antisynthetase autoantibodies". Reumatologia. 58 (1). Termedia Sp. z.o.o.: 4–8. doi:10.5114/reum.2020.93505. PMC 7174798. PMID 32322117.
  16. ^ Katz A, Bena J, Chatterjee S (October 21, 2018). "Antisynthetase Syndrome: Prevalence of Serositis in Autoantibody Subsets". Arthritis Rheumatol. 70 (9). Retrieved 1 December 2023.
  17. ^ a b c Hervier B, Devilliers H, Stanciu R, Meyer A, Uzunhan Y, Masseau A, et al. (December 2012). "Hierarchical cluster and survival analyses of antisynthetase syndrome: phenotype and outcome are correlated with anti-tRNA synthetase antibody specificity". Autoimmunity Reviews. 12 (2). Elsevier BV: 210–217. doi:10.1016/j.autrev.2012.06.006. PMID 22771754.
  18. ^ a b Chatterjee S, Prayson R, Farver C (October 2013). "Antisynthetase syndrome: not just an inflammatory myopathy". Cleveland Clinic Journal of Medicine. 80 (10): 655–666. doi:10.3949/ccjm.80a.12171. PMID 24085811.
  19. ^ Opinc AH, Makowska JS (February 2021). "Antisynthetase syndrome — much more than just a myopathy". Seminars in Arthritis and Rheumatism. 51 (1). Elsevier BV: 72–83. doi:10.1016/j.semarthrit.2020.09.020. PMID 33360231. S2CID 229694735. Retrieved December 4, 2023.
  20. ^ a b Marie I, Hatron PY, Dominique S, Cherin P, Mouthon L, Menard JF, et al. (June 2012). "Short-term and long-term outcome of anti-Jo1-positive patients with anti-Ro52 antibody". Seminars in Arthritis and Rheumatism. 41 (6). Elsevier BV: 890–899. doi:10.1016/j.semarthrit.2011.09.008. PMID 22078416. Retrieved December 4, 2023.
  21. ^ a b Klein M, Mann H, Vencovský J (December 2019). "Arthritis in Idiopathic Inflammatory Myopathies". Current Rheumatology Reports. 21 (12). Springer Science and Business Media LLC: 70. doi:10.1007/s11926-019-0878-x. PMID 31813070. S2CID 208767855. Retrieved December 4, 2023.
  22. ^ Guillochon-Petitcuenot C, Bierry G, Maurier F, Afif N, Messer L, Gottenberg JE, Sibilia J, Meyer A (2018). AB0742 Hand x-ray lesions are frequent in antisynthetase syndrome patients with arthralgia and increase with the radiographic follow-up, whatever the extra-articular features and the serotype of antisynthetase syndrome. BMJ Publishing Group Ltd and European League Against Rheumatism. doi:10.1136/annrheumdis-2018-eular.4602. Retrieved December 1, 2023.
  23. ^ Block JA, Sequeira W (June 2001). "Raynaud's phenomenon". Lancet. 357 (9273). Elsevier BV: 2042–2048. doi:10.1016/s0140-6736(00)05118-7. PMID 11438158. S2CID 27272970. Retrieved December 4, 2023.
  24. ^ Gayraud M (January 2007). "Raynaud's phenomenon". Joint Bone Spine. 74 (1). Elsevier BV: e1–e8. doi:10.1016/j.jbspin.2006.07.002. PMID 17218139. Retrieved December 4, 2023.
  25. ^ Bugatti L, De Angelis R, Filosa G, Salaffi F (2005). "Bilateral, asymptomatic scaly and fissured cutaneous lesions of the fingers in a patient presenting with myositis". Indian Journal of Dermatology, Venereology and Leprology. 71 (2). Scientific Scholar: 137–138. doi:10.4103/0378-6323.14009. hdl:1807/5500. PMID 16394397. S2CID 6102838.
  26. ^ Lega JC, Fabien N, Reynaud Q, Durieu I, Durupt S, Dutertre M, et al. (September 2014). "The clinical phenotype associated with myositis-specific and associated autoantibodies: a meta-analysis revisiting the so-called antisynthetase syndrome". Autoimmunity Reviews. 13 (9). Elsevier BV: 883–891. doi:10.1016/j.autrev.2014.03.004. PMID 24704867. Retrieved December 4, 2023.
  27. ^ González-Pérez MI, Mejía-Hurtado JG, Pérez-Román DI, Buendía-Roldán I, Mejía M, Falfán-Valencia R, et al. (March 2020). "Evolution of Pulmonary Function in a Cohort of Patients with Interstitial Lung Disease and Positive for Antisynthetase Antibodies". The Journal of Rheumatology. 47 (3): 415–423. doi:10.3899/jrheum.181141. PMID 31203227. S2CID 189945185. Retrieved December 4, 2023.
  28. ^ Zhang Y, Ge Y, Yang H, Chen H, Tian X, Huang Z, et al. (August 2020). "Clinical features and outcomes of the patients with anti-glycyl tRNA synthetase syndrome". Clinical Rheumatology. 39 (8). Springer Science and Business Media LLC: 2417–2424. doi:10.1007/s10067-020-04979-8. PMID 32144624. S2CID 212421153. Retrieved December 4, 2023.
  29. ^ a b Hervier B, Meyer A, Dieval C, Uzunhan Y, Devilliers H, Launay D, et al. (November 2013). "Pulmonary hypertension in antisynthetase syndrome: prevalence, aetiology and survival". The European Respiratory Journal. 42 (5). European Respiratory Society (ERS): 1271–1282. doi:10.1183/09031936.00156312. PMID 23397301.
  30. ^ Dieval C, Deligny C, Meyer A, Cluzel P, Champtiaux N, Lefevre G, et al. (July 2015). "Myocarditis in Patients With Antisynthetase Syndrome: Prevalence, Presentation, and Outcomes". Medicine. 94 (26). Ovid Technologies (Wolters Kluwer Health): e798. doi:10.1097/md.0000000000000798. PMC 4504539. PMID 26131832.
  31. ^ Ernst A, Schlattmann P, Waldfahrer F, Westhofen M (August 2017). "Die Behandlung des M. Menière mit Betahistin: Kritische Anmerkungen zur BEMED-Studie" [The treatment of Menière's disease with betahistine: Critical comments on the BEMED study]. Laryngo- Rhino- Otologie (in German). 96 (8). Georg Thieme Verlag KG: 519–521. doi:10.1055/s-0043-113690. PMID 28850992.
  32. ^ Nishikai M, Reichlin M (August 1980). "Heterogeneity of precipitating antibodies in polymyositis and dermatomyositis. Characterization of the Jo-1 antibody system". Arthritis and Rheumatism. 23 (8): 881–888. doi:10.1002/art.1780230802. PMID 7406938.
  33. ^ Lazarou, Ilias N.; Guerne, Pierre-André (March 15, 2013). "Classification, Diagnosis, and Management of Idiopathic Inflammatory Myopathies". The Journal of Rheumatology. 40 (5): 550–564. doi:10.3899/jrheum.120682. ISSN 0315-162X. PMID 23504386. S2CID 20990459.
  34. ^ Connors GR, Christopher-Stine L, Oddis CV, Danoff SK (December 2010). "Interstitial lung disease associated with the idiopathic inflammatory myopathies: what progress has been made in the past 35 years?". Chest. 138 (6): 1464–1474. doi:10.1378/chest.10-0180. PMID 21138882.
  35. ^ Bahmer T, Romagnoli M, Girelli F, Claussen M, Rabe KF (April 2016). "The use of auto-antibody testing in the evaluation of interstitial lung disease (ILD)--A practical approach for the pulmonologist". Respiratory Medicine. 113: 80–92. doi:10.1016/j.rmed.2016.01.019. PMID 26921132.
  36. ^ Chen Z, Cao M, Plana MN, Liang J, Cai H, Kuwana M, Sun L (August 2013). "Utility of anti-melanoma differentiation-associated gene 5 antibody measurement in identifying patients with dermatomyositis and a high risk for developing rapidly progressive interstitial lung disease: a review of the literature and a meta-analysis". Arthritis Care & Research. 65 (8): 1316–1324. doi:10.1002/acr.21985. PMID 23908005.
  37. ^ a b Targoff IN (November 2002). "Laboratory testing in the diagnosis and management of idiopathic inflammatory myopathies". Rheumatic Disease Clinics of North America. 28 (4): 859–90, viii. doi:10.1016/s0889-857x(02)00032-7. PMID 12506776. Retrieved December 4, 2023.
  38. ^ La Corte R, Lo Mo Naco A, Locaputo A, Dolzani F, Trotta F (May 2006). "In patients with antisynthetase syndrome the occurrence of anti-Ro/SSA antibodies causes a more severe interstitial lung disease". Autoimmunity. 39 (3): 249–253. doi:10.1080/08916930600623791. PMID 16769659. S2CID 41393193. Retrieved December 4, 2023.
  39. ^ Mileti LM, Strek ME, Niewold TB, Curran JJ, Sweiss NJ (August 2009). "Clinical characteristics of patients with anti-Jo-1 antibodies: a single center experience". Journal of Clinical Rheumatology. 15 (5): 254–255. doi:10.1097/RHU.0b013e3181b0e910. PMC 3380442. PMID 19590436.
  40. ^ Debray MP, Borie R, Revel MP, Naccache JM, Khalil A, Toper C, et al. (March 2015). "Interstitial lung disease in anti-synthetase syndrome: initial and follow-up CT findings". European Journal of Radiology. 84 (3): 516–523. doi:10.1016/j.ejrad.2014.11.026. PMID 25541020. Retrieved December 4, 2023.
  41. ^ Travis WD, Costabel U, Hansell DM, King TE, Lynch DA, Nicholson AG, et al. (September 2013). "An official American Thoracic Society/European Respiratory Society statement: Update of the international multidisciplinary classification of the idiopathic interstitial pneumonias". American Journal of Respiratory and Critical Care Medicine. 188 (6): 733–748. doi:10.1164/rccm.201308-1483ST. PMC 5803655. PMID 24032382.
  42. ^ Yousem SA, Gibson K, Kaminski N, Oddis CV, Ascherman DP (June 2010). "The pulmonary histopathologic manifestations of the anti-Jo-1 tRNA synthetase syndrome". Modern Pathology. 23 (6): 874–880. doi:10.1038/modpathol.2010.65. PMID 20228783.
  43. ^ Dalakas MC (November 2002). "Muscle biopsy findings in inflammatory myopathies". Rheumatic Disease Clinics of North America. 28 (4): 779–98, vi. doi:10.1016/s0889-857x(02)00030-3. PMID 12506772. Retrieved December 4, 2023.
  44. ^ Joffe MM, Love LA, Leff RL, Fraser DD, Targoff IN, Hicks JE, et al. (April 1993). "Drug therapy of the idiopathic inflammatory myopathies: predictors of response to prednisone, azathioprine, and methotrexate and a comparison of their efficacy". The American Journal of Medicine. 94 (4): 379–387. doi:10.1016/0002-9343(93)90148-i. PMID 8386437. Retrieved December 4, 2023.
  45. ^ Bunch TW, Worthington JW, Combs JJ, Ilstrup DM, Engel AG (March 1980). "Azathioprine with prednisone for polymyositis. A controlled, clinical trial". Annals of Internal Medicine. 92 (3): 365–369. doi:10.7326/0003-4819-92-3-365. PMID 6986827. Retrieved December 4, 2023.
  46. ^ Fischer A, Brown KK, Du Bois RM, Frankel SK, Cosgrove GP, Fernandez-Perez ER, et al. (May 2013). "Mycophenolate mofetil improves lung function in connective tissue disease-associated interstitial lung disease". The Journal of Rheumatology. 40 (5): 640–646. doi:10.3899/jrheum.121043. PMC 3676865. PMID 23457378.
  47. ^ Cavagna L, Caporali R, Abdì-Alì L, Dore R, Meloni F, Montecucco C (April 2013). "Cyclosporine in anti-Jo1-positive patients with corticosteroid-refractory interstitial lung disease". The Journal of Rheumatology. 40 (4): 484–492. doi:10.3899/jrheum.121026. PMID 23418387. S2CID 207726963. Retrieved December 4, 2023.
  48. ^ Oddis CV, Sciurba FC, Elmagd KA, Starzl TE (May 1999). "Tacrolimus in refractory polymyositis with interstitial lung disease". Lancet. 353 (9166): 1762–1763. doi:10.1016/S0140-6736(99)01927-3. PMC 2977932. PMID 10347992.
  49. ^ Matsubara S, Kondo K, Sugaya K, Miyamoto K (October 2012). "Effects of tacrolimus on dermatomyositis and polymyositis: a prospective, open, non-randomized study of nine patients and a review of the literature". Clinical Rheumatology. 31 (10): 1493–1498. doi:10.1007/s10067-012-2044-y. PMID 22886003. S2CID 11036524. Retrieved December 4, 2023.
  50. ^ Witt LJ, Demchuk C, Curran JJ, Strek ME (February 2016). "Benefit of adjunctive tacrolimus in connective tissue disease-interstitial lung disease". Pulmonary Pharmacology & Therapeutics. 36: 46–52. doi:10.1016/j.pupt.2015.12.004. PMC 4760686. PMID 26762710.
  51. ^ Wilkes MR, Sereika SM, Fertig N, Lucas MR, Oddis CV (August 2005). "Treatment of antisynthetase-associated interstitial lung disease with tacrolimus". Arthritis and Rheumatism. 52 (8): 2439–2446. doi:10.1002/art.21240. PMID 16052580.
  52. ^ Sem M, Molberg O, Lund MB, Gran JT (August 2009). "Rituximab treatment of the anti-synthetase syndrome: a retrospective case series". Rheumatology. 48 (8): 968–971. doi:10.1093/rheumatology/kep157. PMID 19531628. Retrieved December 4, 2023.
  53. ^ Keir GJ, Maher TM, Hansell DM, Denton CP, Ong VH, Singh S, et al. (September 2012). "Severe interstitial lung disease in connective tissue disease: rituximab as rescue therapy". The European Respiratory Journal. 40 (3): 641–648. doi:10.1183/09031936.00163911. PMID 22282550.
  54. ^ Ge Y, Peng Q, Zhang S, Zhou H, Lu X, Wang G (January 2015). "Cyclophosphamide treatment for idiopathic inflammatory myopathies and related interstitial lung disease: a systematic review". Clinical Rheumatology. 34 (1): 99–105. doi:10.1007/s10067-014-2803-z. PMID 25367345. S2CID 37795037.
  55. ^ Mira-Avendano IC, Parambil JG, Yadav R, Arrossi V, Xu M, Chapman JT, Culver DA (June 2013). "A retrospective review of clinical features and treatment outcomes in steroid-resistant interstitial lung disease from polymyositis/dermatomyositis". Respiratory Medicine. 107 (6): 890–896. doi:10.1016/j.rmed.2013.02.015. PMID 23517887.
  56. ^ Dalakas MC, Illa I, Dambrosia JM, Soueidan SA, Stein DP, Otero C, et al. (December 1993). "A controlled trial of high-dose intravenous immune globulin infusions as treatment for dermatomyositis". The New England Journal of Medicine. 329 (27): 1993–2000. doi:10.1056/NEJM199312303292704. PMID 8247075.
  57. ^ Bakewell CJ, Raghu G (February 2011). "Polymyositis associated with severe interstitial lung disease: remission after three doses of IV immunoglobulin". Chest. 139 (2): 441–443. doi:10.1378/chest.10-0360. PMID 21285059. Retrieved December 4, 2023.
  58. ^ Müller F, Boeltz S, Knitza J, Aigner M, Völkl S, Kharboutli S, et al. (March 2023). "CD19-targeted CAR T cells in refractory antisynthetase syndrome". Lancet. 401 (10379). Elsevier: 815–818. doi:10.1016/S0140-6736(23)00023-5. PMID 36930673. S2CID 256874601. Retrieved December 4, 2023.
  59. ^ Lundberg IE, Galindo-Feria AS, Horuluoglu B (June 2023). "CD19-Targeting CAR T-Cell Therapy for Antisynthetase Syndrome". JAMA. 329 (24): 2130–2131. doi:10.1001/jama.2023.7240. PMID 37367988. S2CID 259259257. Retrieved December 4, 2023.
  60. ^ a b Marie I, Hatron PY, Cherin P, Hachulla E, Diot E, Vittecoq O, et al. (October 2013). "Functional outcome and prognostic factors in anti-Jo1 patients with antisynthetase syndrome". Arthritis Research & Therapy. 15 (5): R149. doi:10.1186/ar4332. PMC 3978997. PMID 24286268.
  61. ^ Delplanque M, Gatfosse M, Ait-Oufella H, Mercier O, Savale L, Fain O, Mekinian A (September 2018). "Bi-lung transplantation in anti-synthetase syndrome with life-threatening interstitial lung disease". Rheumatology. 57 (9): 1688–1689. doi:10.1093/rheumatology/key123. PMID 29718458. Retrieved December 4, 2023.
  62. ^ Alexanderson H (July 2016). "Physical exercise as a treatment for adult and juvenile myositis". Journal of Internal Medicine. 280 (1): 75–96. doi:10.1111/joim.12481. PMID 26854121.
  63. ^ a b c Rojas-Serrano, Jorge; Herrera-Bringas, Denisse; Mejía, Mayra; Rivero, Hermes; Mateos-Toledo, Heidegger; Figueroa, José E. (2015). "Prognostic factors in a cohort of antisynthetase syndrome (ASS): serologic profile is associated with mortality in patients with interstitial lung disease (ILD)". Clinical Rheumatology. 34 (9): 1563–1569. doi:10.1007/s10067-015-3023-x. ISSN 0770-3198. PMID 26219488. S2CID 12012669. Retrieved December 4, 2023.
  64. ^ Marie, I.; Josse, S.; Decaux, O.; Dominique, S.; Diot, E.; Landron, C.; Roblot, P.; Jouneau, S.; Hatron, P.Y.; Tiev, K.P.; Vittecoq, O.; Noel, D.; Mouthon, L.; Menard, J.-F.; Jouen, F. (2012). "Comparison of long-term outcome between anti-Jo1- and anti-PL7/PL12 positive patients with antisynthetase syndrome". Autoimmunity Reviews. 11 (10). Elsevier BV: 739–745. doi:10.1016/j.autrev.2012.01.006. ISSN 1568-9972. PMID 22326685. Retrieved December 4, 2023.
  65. ^ Rozelle, Andrew; Trieu, Sandy; Chung, Lorinda (2008). "Malignancy in the Setting of the Anti-Synthetase Syndrome". JCR: Journal of Clinical Rheumatology. 14 (5). Ovid Technologies (Wolters Kluwer Health): 285–288. doi:10.1097/rhu.0b013e31817d116f. ISSN 1076-1608. PMID 18664993. Retrieved December 4, 2023.
  66. ^ Legault, Dominic; McDermott, John; Crous-Tsanaclis, Ana Maria; Boire, Gilles (January 1, 2008). "Cancer-associated myositis in the presence of anti-Jo1 autoantibodies and the antisynthetase syndrome". The Journal of Rheumatology. 35 (1): 169–171. ISSN 0315-162X. PMID 18176990. Retrieved December 4, 2023.
  67. ^ Castañeda-Pomeda, Marta; Prieto-González, Sergio; Grau, Josep Maria (2011). "Antisynthetase Syndrome and Malignancy". JCR: Journal of Clinical Rheumatology. 17 (8). Ovid Technologies (Wolters Kluwer Health): 458. doi:10.1097/rhu.0b013e31823b1878. ISSN 1076-1608. PMID 22126809. Retrieved December 4, 2023.
  68. ^ Zang, Yuan-Sheng; Xiu, Qing-Yu; Fang, Zheng; Li, Bing; Xia, Tian-Bao (January 1, 2008). "Case Report: Dramatic Recovery of Lung Adenocarcinoma–Associated Dermatomyositis with Targeted Lung Cancer Therapy Alone". The Oncologist. 13 (1). Oxford University Press (OUP): 79–81. doi:10.1634/theoncologist.2007-0172. ISSN 1083-7159. PMID 18245014.
  69. ^ Noguchi, Eri; Uruha, Akinori; Suzuki, Shigeaki; Hamanaka, Kohei; Ohnuki, Yuko; Tsugawa, Jun; Watanabe, Yurika; Nakahara, Jin; Shiina, Takashi; Suzuki, Norihiro; Nishino, Ichizo (August 1, 2017). "Skeletal Muscle Involvement in Antisynthetase Syndrome". JAMA Neurology. 74 (8). American Medical Association (AMA): 992–999. doi:10.1001/jamaneurol.2017.0934. ISSN 2168-6149. PMC 5710328. PMID 28586844.
  70. ^ Ghirardello, A.; Zampieri, S.; Tarricone, E.; Iaccarino, L.; Bendo, R.; Briani, C.; Rondinone, R.; Sarzi-Puttini, P.; Todesco, S.; Doria, A. (2006). "Clinical implications of autoantibody screening in patients with autoimmune myositis". Autoimmunity. 39 (3): 217–221. doi:10.1080/08916930600622645. ISSN 0891-6934. PMID 16769655. S2CID 2411394. Retrieved December 4, 2023.

Further reading

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